Suppression of experimental autoimmune myasthenia gravis by inhibiting the signaling between IFN-γ inducible protein 10 (IP-10) and its receptor CXCR3

Tali Feferman; Revital Aricha; Keren Mizrachi; Erez Geron; Ronen Alon; Miriam C. Souroujon; Sara Fuchs

doi:10.1016/j.jneuroim.2009.01.021

Suppression of experimental autoimmune myasthenia gravis by inhibiting the signaling between IFN-γ inducible protein 10 (IP-10) and its receptor CXCR3

Tali Feferman, Revital Aricha, Keren Mizrachi, Erez Geron, Ronen Alon, Miriam C. Souroujon, Sara Fuchs

Life Sciences discipline

Research output: Contribution to journal › Article › peer-review

Abstract

We have previously demonstrated that the chemokine IFN-γ inducible protein 10 (IP-10) and its receptor CXCR3, are overexpressed in myasthenia gravis (MG) and its animal model experimental autoimmune MG (EAMG). We now studied the potential of modulating rat EAMG by interference in CXCR3/IP-10 signaling. Two different approaches were used: 1) blocking IP-10 by IP-10-specific antibodies and 2) inhibiting the CXCR3 chemokine receptor by a CXCR3 antagonist. Treatment by either of these reagents led to suppression of EAMG suggesting that inhibition of CXCR3/IP-10 signaling can be considered as a potential treatment modality for MG.

Original language	English
Pages (from-to)	87-95
Number of pages	9
Journal	Journal of Neuroimmunology
Volume	209
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2009.01.021
State	Published - 30 Apr 2009

Bibliographical note

Funding Information:
This research was supported by grants from The Muscular Dystrophy Association of America (MDA), The Association Francaise Contre les Myopathies (AFM), The European Commission (LSHN-CT-2006-037833) and The Chief Scientist Office, Israel Ministry of Health.

Keywords

CXCR3
Experimental autoimmune myasthenia gravis (EAMG)
IFN-γ inducible protein 10 (IP-10)
Immunosuppression
Myasthenia gravis (MG)

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10.1016/j.jneuroim.2009.01.021

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title = "Suppression of experimental autoimmune myasthenia gravis by inhibiting the signaling between IFN-γ inducible protein 10 (IP-10) and its receptor CXCR3",

abstract = "We have previously demonstrated that the chemokine IFN-γ inducible protein 10 (IP-10) and its receptor CXCR3, are overexpressed in myasthenia gravis (MG) and its animal model experimental autoimmune MG (EAMG). We now studied the potential of modulating rat EAMG by interference in CXCR3/IP-10 signaling. Two different approaches were used: 1) blocking IP-10 by IP-10-specific antibodies and 2) inhibiting the CXCR3 chemokine receptor by a CXCR3 antagonist. Treatment by either of these reagents led to suppression of EAMG suggesting that inhibition of CXCR3/IP-10 signaling can be considered as a potential treatment modality for MG.",

keywords = "CXCR3, Experimental autoimmune myasthenia gravis (EAMG), IFN-γ inducible protein 10 (IP-10), Immunosuppression, Myasthenia gravis (MG)",

author = "Tali Feferman and Revital Aricha and Keren Mizrachi and Erez Geron and Ronen Alon and Souroujon, {Miriam C.} and Sara Fuchs",

note = "Funding Information: This research was supported by grants from The Muscular Dystrophy Association of America (MDA), The Association Francaise Contre les Myopathies (AFM), The European Commission (LSHN-CT-2006-037833) and The Chief Scientist Office, Israel Ministry of Health.",

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doi = "10.1016/j.jneuroim.2009.01.021",

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AU - Feferman, Tali

AU - Aricha, Revital

AU - Mizrachi, Keren

AU - Geron, Erez

AU - Alon, Ronen

AU - Souroujon, Miriam C.

AU - Fuchs, Sara

N1 - Funding Information: This research was supported by grants from The Muscular Dystrophy Association of America (MDA), The Association Francaise Contre les Myopathies (AFM), The European Commission (LSHN-CT-2006-037833) and The Chief Scientist Office, Israel Ministry of Health.

PY - 2009/4/30

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N2 - We have previously demonstrated that the chemokine IFN-γ inducible protein 10 (IP-10) and its receptor CXCR3, are overexpressed in myasthenia gravis (MG) and its animal model experimental autoimmune MG (EAMG). We now studied the potential of modulating rat EAMG by interference in CXCR3/IP-10 signaling. Two different approaches were used: 1) blocking IP-10 by IP-10-specific antibodies and 2) inhibiting the CXCR3 chemokine receptor by a CXCR3 antagonist. Treatment by either of these reagents led to suppression of EAMG suggesting that inhibition of CXCR3/IP-10 signaling can be considered as a potential treatment modality for MG.

AB - We have previously demonstrated that the chemokine IFN-γ inducible protein 10 (IP-10) and its receptor CXCR3, are overexpressed in myasthenia gravis (MG) and its animal model experimental autoimmune MG (EAMG). We now studied the potential of modulating rat EAMG by interference in CXCR3/IP-10 signaling. Two different approaches were used: 1) blocking IP-10 by IP-10-specific antibodies and 2) inhibiting the CXCR3 chemokine receptor by a CXCR3 antagonist. Treatment by either of these reagents led to suppression of EAMG suggesting that inhibition of CXCR3/IP-10 signaling can be considered as a potential treatment modality for MG.

KW - CXCR3

KW - Experimental autoimmune myasthenia gravis (EAMG)

KW - IFN-γ inducible protein 10 (IP-10)

KW - Immunosuppression

KW - Myasthenia gravis (MG)

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Suppression of experimental autoimmune myasthenia gravis by inhibiting the signaling between IFN-γ inducible protein 10 (IP-10) and its receptor CXCR3

Abstract

Bibliographical note

Keywords

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